Researchers demonstrated that KRAS mutations, common in CMS3 CRC subtype, promote an immunosuppressive TME, inducing the conversion of CD4+ cells to Tregs [26, 27•] and, by upregulation of CXCL3 expression, the main ligand of CXCR2 on MDSCs surface, support their migration inside tumor core [28]. The gene discussed is CD4; the disease is neoplasm.